Heather B. Bradshaw

This study examines how morphine alters lipid levels in different brain and body regions after acute or chronic administration, identifying potential endogenous lipid signaling systems involved in opioid reward and withdrawal.

This study investigates psilocybin's effects on repetitive mild head injury in rats, showing reductions in edema, improved vascular function, and modulation of neuroinflammatory and neuroplasticity markers.

This study shows acetaminophen reduces pain by altering lipid signaling via cannabinoid receptors and enzymes in mice.

The paper identifies compartment-specific changes in endolipid signaling during psoriasiform inflammation using lipidomic and transcriptomic analyses in mouse models.

This study shows that perinatal CBD exposure alters astrocyte morphology and tripartite synapse organization in a sex-dependent manner in the medial prefrontal cortex.

This study examines sex differences in plasma endocannabinoid and lipid levels in a rat model of acute and repeated mTBI, finding greater changes in males and potential biomarker value for mTBI outcomes.

The paper shows acetaminophen inhibits DAGLα, reducing 2-arachidonoyl glycerol production and suggesting a novel antinociceptive mechanism involving DAGLα/CB1 circuits.

This paper investigates the role of NAPE-PLD in the ventral tegmental area, showing its impact on reward behaviors, feeding, and energy homeostasis through transcriptomic analysis and genetic manipulations.

This study examines the effects of combined alcohol and THC use on working memory in rats, finding no significant impact on memory tasks despite THC reducing ethanol intake.

The paper identifies 2-linoleoyl glycerol (2-LG) as an endocannabinoid activated by light in Drosophila photoreceptor cells, which in turn activates TRPC channels.

This study examines how early-life stress affects cerebellar endocannabinoid levels and behavior, revealing sex-specific differences and potential contributions to brain sexual differentiation.

This study shows that astrocytes release lipids like PGE2 through a Ca2+-independent pathway, increasing neuronal excitability by inhibiting Kv channels.